Mechanisms of postprandial hyperlipidaemia--remnants and coronary artery disease.

High plasma concentrations of triglyceride-rich lipoprotein are associated with an increased risk of coronary artery disease (CAD). In the postprandial state, there is a large increase in chylomicron and very low-density lipoprotein (VLDL) concentrations. The accumulation of potentially atherogenic particles is controlled by the balance of their synthesis and clearance. Chylomicrons are rich in triglyceride and secreted by the intestine postprandially. Chylomicrons compete with VLDL for hydrolysis by lipoprotein lipase (LPL). This competition may cause the increase in large plasma concentration of VLDL seen in the postprandial state. Postprandial increases in atherogenic plasma lipoprotein concentrations are accentuated in insulin-resistant states. Insulin resistance is associated with greater flux of free fatty acids, which may in turn lead to enhanced synthesis of VLDL. Alimentary lipidaemia has been shown to effect changes in the coagulation cascade which may provide additional connections between postprandial lipaemia and CAD. Thus, specific postprandial changes in plasma lipids may be indicative of atherogenic risk. Measurement of postprandial plasma triglyceride concentration and the apo B-48 and apo B-100 contents in triglyceride-rich lipoprotein fractions are probably useful indicators of postprandial dyslipidaemia, but prospective studies of how these lipid variables relate to CAD progression are needed.